Abortive infection by human cytomegalovirus (CMV) of guinea pig embryo (GP) cells in culture induces an increase in the rate of synthesis of cellular components (including DNA) similar to that demonstrated for other viruses that are known to cause cellular transformation. An understanding of the mechanism by which CMV stimulates the synthesis of cellular components and leads to abortive infection may give information about oncogenic functions of the virus. Our recent findings indicate that the block in the infective process of CMV in GP cells is at a step prior to the initiation of viral DNA replication and that there is a gradual decrease of density of input viral DNA during this abortive infection. These findings provide a basis for further investigation of the interaction between CMV and its host cells. Thus, this project proposes: 1) to study the factor(s) at the transcriptional and translational levels that are involved in blocking viral replication in abortive infection, and 2) to determine if the mechanism that causes the decrease of density of input viral genome is due to the linkage of viral DNA to cellular DNA or to the association of viral DNA with other substance(s) such as protein, glycoprotein, etc. which may be coded by cells or by the virus.